Basic Information
| LncRNA/CircRNA Name | circ_0067934 |
| Synonyms | |
| Region | |
| Ensemble | |
| Refseq |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | Drug | |||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | cervical cancer |
| ICD-0-3 | C53 |
| Methods | qPCR, Cell proliferation assay, Transwell assay, Luciferase reporter assay, In vivo experiments |
| Sample | CC tissues, CC cell lines SiHa, CaSki, Hela, and C4?? and immortalized cervical epithelium NC104 |
| Expression Pattern | up-regulated |
| Function Description | circ_0067934 was overexpressed in CC tissues and cell lines. Circ_0067934 upregulation was associated with advanced stage, lymph node metastasis, and poor prognosis in CC patients. Knockdown of circ_0067934 suppressed the proliferation, colony formation, migration, invasion, and epithelial mesenchymal transition of CC cells in vitro. Circ_0067934 loss also inhibited CC tumor growth in vivo. Mechanistically, silencing circ_0067934 increased miR 545 expression. MiR 545 repressed EIF3C expression through targeting its 3 untranslated region. MiR 545 suppressed the proliferation, migration, and invasion of CC cells, whereas restoration of EIF3C could rescue the effects of circ_0067934 knockdown. Taken together, our findings revealed that circ_0067934 promotes CC progression via miR 545/EIF3C axis. Our study may provide a new insight into the pathogenesis of CC. |
| Pubmed ID | 30362562 |
| Year | 2018 |
| Title | Overexpressed circ_0067934 acts as an oncogene to facilitate cervical cancer progression via the miR??45/EIF3C axis |
External Links
| Links for circ_0067934 | GenBank HGNC NONCODE |
| Links for cervical cancer | OMIM COSMIC |